Clinical-grade preparation of human natural regulatory T-cells encoding the thymidine kinase suicide gene as a safety gene

J Gene Med. 2008 Aug;10(8):834-46. doi: 10.1002/jgm.1220.

Abstract

Background: Human CD4+CD25+FOXP3+ natural regulatory T-cells (nTreg) have a great therapeutic potential for the induction of tolerance in allo-transplanted patients or for the control of severe auto-immune diseases. However, clinical-grade production of nTreg remains difficult to achieve because of the absence of a truly specific surface marker and of their low frequency that implies a need for their ex vivo expansion. Furthermore, safety issues should be taken into consideration due to the risk of either uncontrolled nTreg-induced immunosuppression or uncontrolled proliferation of autoreactive contaminating T-cells particularly in an auto-immune context.

Methods: We compared different clinical-grade conditions for immuno-magnetic selection and ex vivo expansion of nTreg. For safety, expanded cells were genetically modified with retroviral vectors co-expressing human CD90 and HSV1 thymidine kinase. The CD90 surface marker and thymidine kinase allow for selection and elimination of transduced cells by ganciclovir, respectively.

Results: We showed that (i) nTreg could be enriched in a one step using CD25 microbeads, were functionally suppressive and mainly FOXP3+; (ii) using anti-CD28- and anti-CD3-coated beads, interleukin-2 and rapamycin, nTreg were expanded 150-200-fold after 3 weeks. Under these clinical-grade conditions, they remained suppressive, and no major alteration of the TCR repertoire was observed; (iii) after efficient retroviral transduction and CD90 selection, nTreg maintained their suppressive activity; (iv) transduced nTreg could be eliminated by ganciclovir upon activation.

Conclusions: The efficient procedure reported here for the preparation of nTreg, whose safety has been ensured, is now applicable for further clinical trials.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antibodies, Monoclonal / immunology
  • CD4-Positive T-Lymphocytes / immunology
  • Cell Death / genetics
  • Cell Proliferation / drug effects
  • Cell Survival / drug effects
  • Cells, Cultured
  • Forkhead Transcription Factors / metabolism
  • Ganciclovir / pharmacology
  • Genes, Transgenic, Suicide / genetics*
  • Genetic Vectors
  • Herpesvirus 1, Human / enzymology
  • Humans
  • Immunomagnetic Separation
  • Immunosuppressive Agents / pharmacology
  • Interleukin-2 / pharmacology
  • Interleukin-2 Receptor alpha Subunit / metabolism
  • Interleukin-7 Receptor alpha Subunit / metabolism
  • Lymphocyte Activation / drug effects
  • Microspheres
  • Retroviridae / genetics*
  • Sirolimus / pharmacology
  • T-Lymphocytes, Regulatory / drug effects
  • T-Lymphocytes, Regulatory / immunology*
  • Thy-1 Antigens / genetics*
  • Thymidine Kinase / genetics*
  • Time Factors
  • Transduction, Genetic

Substances

  • Antibodies, Monoclonal
  • FOXP3 protein, human
  • Forkhead Transcription Factors
  • Immunosuppressive Agents
  • Interleukin-2
  • Interleukin-2 Receptor alpha Subunit
  • Interleukin-7 Receptor alpha Subunit
  • Thy-1 Antigens
  • Thymidine Kinase
  • Ganciclovir
  • Sirolimus